In vivo and in vitro studies on cold-induced airway response in normal and sensitized rabbits.

We measured the changes in lung resistance (RL) induced by cool inspired air under dry air conditions in anesthetized, paralyzed and artificially ventilated rabbits. We compared the airway response to cold air in non-sensitized (NS) animals with the response in rabbits sensitized (S) to bovine serum albumin. Using in vitro tracheal preparations from the same animals, we observed the effects of lowering the bath temperature on smooth muscle tension and also the response to acetylcholine (Ach). Dose-response curves to Ach were constructed and analyzed in terms of maximal contraction (delta Tmax) and pD2 coefficient (negative logarithm of the molar concentration of Ach producing 50% of maximum contraction). The magnitude of cold induced airway response tested in vivo was significantly greater in S (delta RL = +52% +/- 2) than in NS rabbits (+30% +/- 4; P less than 0.01). In vitro the decrease of temperature in the bathing medium induced a significant relaxation of tracheal spirals in both NS and S preparations (delta T = -2.42 +/- 0.34 g/mg wet tissue, -3.36 +/- 0.8 g/mg wet tissue, respectively). However, an adaptation of this response occurred after 8 min in NS rabbits whereas relaxation persisted in S rabbits. The tracheal contractile response to Ach was decreased by bath cooling in S ans NS animals (delta Tmax = 5.53 +/- 0.15 g/mg wet tissue and 5.03 +/- 0.27 g/mg wet tissue at 37 degrees C; 3.05 +/- 0.30 g/mg wet tissue and 1.93 +/- 0.35 g/mg wet tissue at 17 degrees C, respectively). Moreover, cooling also reduced the velocity of response. In all cases, S preparations displayed hyperresponsiveness to Ach and this was observed for maximal changes in tension as well as for pD2 values. Present observations show that cold induces different effects on airway smooth muscle with the production of a contractile response in in vivo preparations but relaxes isolated tracheal spirals. They also suggest that sensitization by foreign proteins may modify the intrinsic properties of tracheal smooth muscle.